Gene transfer of endothelial nitric oxide synthase, but not Cu/Zn superoxide dismutase, restored nitric oxide availability in the stroke-prone spontaneously hypertensive rat.
Does adenoviral-mediated gene transfer of human eNOS or Cu/ZnSOD improve endothelial function in the SHRSP model?
Gene transfer of eNOS, but not Cu/ZnSOD, restores nitric oxide availability in the stroke-prone spontaneously hypertensive rat model.
Objective: Previous studies from our group have shown a deficit in nitric oxide (NO) bioavailability and an excess production of the 2 superoxide anion (O ) in the stroke prone spontaneously hypertensive rat (SHRSP) compared to the normotensive Wistar Kyoto (WKY) 2 strain. This present study has investigated whether adenoviral-mediated gene transfer of human eNOS or Cu / ZnSOD can alter the 2 NO / O balance, thereby improving endothelial function. Methods: A recombinant adenovirus, Ad / Hu / eNOS, containing the human 2 eNOS cDNA fragment was generated by homologous recombination in 293 cells. Ad / Hu / eNOS or Ad / Cu / ZnSOD was delivered into 9 1 0
M. Yvonne Alexander (Fri,) conducted a other in Stroke prone spontaneously hypertensive rat (SHRSP). Adenoviral-mediated gene transfer of human eNOS or Cu/ZnSOD was evaluated on Nitric oxide/superoxide anion balance and endothelial function. Gene transfer of endothelial nitric oxide synthase, but not Cu/Zn superoxide dismutase, restored nitric oxide availability in the stroke-prone spontaneously hypertensive rat.